These results buttressed previous findings and confirmed that S100A9 exerts a protective role in septic AKI, as indicated by the reduction of animal mortality and improvement of renal dysfunction and pathological changes including cell apoptosis, oxidative stress, and inflammatory response in CLP-treated mice (Figures 2–4), confirming that S100A9 critically contributes to CLP-induced AKI and abnormal kidney function. The gene discussed is S100A9; the disease is acute kidney injury.